Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physiological roles have been suggested for prostacyclin in the cardiovascular system. Prostacyclin was administered by intravenous infusion to unanesthetized rats. Over a 24 hr period, 0.32 mg/kg/day caused only flushing of the ears. Larger doses (0.56 and 1 mg/kg/day) caused hypothermia, behavioral depression, and swelling of the paws. Cumulative dose-response curves for its depressor action were determined in both unanesthetized and anesthetized, vagotomized, ganglion-blocked rats. In unanesthetized rats, the threshold dose was about 0.1 ug/kg/min. Respiratory depression precluded doses larger than 1 ug/kg/min. In anesthetized rats, the threshold dose was about 0.001 ug/kg/min, and the maximally effective dose was about 0.1 micrograms/kg/min. At 0.032 ug/kg/min, blood pressure first fell and then rose slightly. This compensatory rise did not occur in nephrectomized rats, suggesting renin release as the mechanism. Intravenous infusion of 0.1 but not 0.01 ug/kg/min in unanesthetized rats doubled plasma renin activity. In saline-loaded unanesthetized rats, urine volume and urinary sodium excretion were decreased by 0.1 ug/kg/min of prostacyclin.
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PMID:The cardiovascular pharmacology of prostacyclin (PGI2) in the rat. 37 17

This study was performed to investigate the pulmonary vascular reactivity during hypothermia. It was found that the pulmonary vessels were more sensitive to alveolar hypoxia in hypothermic dogs, and that hypoxic pulmonary vasoconstriction (HPV) was enhanced, which could be inhibited by alpha 1-adrenoceptor blocker prazosin. The concentration of arterial plasma norepinephrine (NE) increased in dogs with hypothermia or in those with hypothermia plus hypoxia, but there was no significant difference between these two groups. The plasma level of 5-hydroxytryptamine (5-HT) was reduced during hypoxia in hypothermic dogs. Increase in plasma 6-keto-PGF1 alpha, which appeared in hypoxic dogs, was not observed during hypoxia in hypothermic dogs. These findings suggest that a potentiation in the sensitivity and reactivity of alpha-adrenoceptor in pulmonary vessels and a decrease in the modulation of PGI2 might be responsible for the enhancement of HPV. 5-HT seemed not to play a contributing role in the alteration of HPV.
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PMID:Alteration in hypoxic pulmonary vasoconstriction during hypothermia in dogs. 145 1

Continuous haemofiltration (CHF) mimics physiological glomerular filtration. Blood flows through a haemofilter, which is permeable to water and to all those substances not bound to plasma proteins, of up to about 6,000 d molecular weight. Ten to twenty liters of ultrafiltrate (UF) can be filtered daily. Solute concentration in this UF is very similar to that in plasma water. Because of the large volumes involved, the UF must be replaced continuously with an electrolyte solution. Electrolyte and acid-base disturbances can thus be easily and rapidly corrected. There are different techniques of CHF. Continuous arteriovenous haemofiltration (CAVH) avoids the use of an external blood pump, as the patient's own arterial pressure is used to drive the blood through the filter via a large-bore arterial catheter. On the other hand, continuous venovenous haemofiltration (CVVH) requires the use of a blood pump with a pressure alarm and an air bubble detector. Supplementary diffusive transport [CAVH(D),CVVH(D)] can improve the clearance of low molecular weight toxins, such as urea. In these techniques, there is a continuous flow of dialysate in the UF compartment of the haemofilter. One of the major problems with CHF is the anticoagulation of patients who are at risk of developing haemorrhagic complications. Unfractionated heparin is used most often, but other drugs have been used: low molecular weight heparin, prostacyclin, nafamostat, or sodium citrate. The neutralization of heparin has also been suggested. Because the fluid balance can be easily managed by CHF, patients in acute renal failure can be given standard intravenous feeding. Many small endogenous molecules, such as gastrin, are probably removed by CHF. However, most drugs have a molecular weight less than 6,000 d, and are not totally protein-bound. They are therefore likely to be ultrafiltered, and so, become inefficient. As a result, the drugs used should be adapted to the haemofilter, and vice versa. More than any extracorporeal circulation, CHF increases the incidence of bacterial blood contamination, because of its continuous use. Routine blood cultures should be carried out. Moreover, blood is cooled during its passage in the extracorporeal circuit, leading to hypothermia. There are some devices which prevent this. Renal function can be completely replaced with the production of 12 to 15 l UF a day. CHF must be started early on in the course of the renal failure. When the concentration of blood urea is greater than 40 mmol.l-1 diffuse transport must also be used.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Continuous hemofiltration: an extrarenal filtration method used in intensive care]. 192 60

The effect of prostaglandin I2 (PGI2) on the postischemic recovery of the heart orthotopically transplanted under deep hypothermia was evaluated using puppies. Twenty-four pairs of dogs were divided into 4 groups according to the usage of PGI2 and preservation of the donor heart (in Euro-Collins' solution at 4 degrees C for 4 hours), namely Group I (non PGI2, no preservation), Group II (PGI2-treated, no preservation), Group III (non PGI2, 4 hours preservation), Group IV (PGI2-treated, 4 hours preservation). PGI2 was added into the donor's cardioplegic solution (500 ng/ml) and also was given intravenously to the recipient during cooling and rewarming periods (1 microgram/kg/min), and left ventricular pressure, max dp/dt, cardiac output were continuously monitored, and postmortem studies on myocardium were performed. Results were as follows: PGI2 yielded significantly better recovery of cardiac output and left ventricular pressure after transplanted of the heart, [Group I vs Group II (p less than 0.05), Group III vs Group IV (p less than 0.01)]. This effect was especially remarkable in the preserved heart groups. Microscopically, the contraction band formation in the myocardium was more prominent in Group III than in Group IV. It is concluded that PGI2 is of great use for the postischemic recovery of the transplanted heart not only by ameliorating the myocardial ischemic recovery of the transplanted heart, but also by reducing the afterload of the recipient during the recovery period from deep hypothermia.
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PMID:[The effect of prostaglandin I2 on the postischemic recovery of the transplanted heart under deep hypothermia]. 202 15

Many anesthesia providers involved in orthotopic liver transplantation (OTL) have become increasingly aware of the incidence of hypotension immediately following revascularization of the donor liver. Postreperfusion syndrome (PRS) is usually characterized by a decrease in systemic blood pressure of at least 30 torr with a duration of 5 minutes or more. Several researchers have suggested that the etiology of this hypotension may be related to acute hyperkalemia, acidosis, hypothermia, reflex systemic vasodilation, or some yet unidentified prostaglandin liberated from the gut at reanastomosis. The potential role of prostacyclin as the primary etiologic agent responsible for this syndrome was studied. Serum prostacyclin measurements were obtained in seven patients 1 minute before and 5 minutes after revascularization. Coincident measures were taken of preselected cardiovascular parameters. Five patients demonstrated increased levels of prostacyclin during clamping of the portal vein and four experienced significant hypotension at reperfusion. In the five patients demonstrating hypotension, a decrease in heart rate and systemic vascular resistance and an increase in cardiac output and PCWP was noted. It is concluded that one or more endogenous prostacyclins may play an important role in the etiology of postreperfusion syndrome.
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PMID:Prostacyclin levels during orthotopic liver transplantation. 228 9

The role of Prostaglandin I2 (PGI2) on heart transplantation under deep hypothermia were investigated using 25 weighing an average of 5 kg. They were put to deep hypothermia by surface cooling with either anesthesia until rectal temperature reached 18 degrees C. Then the heart was arrested with cardioplegic solution, removed and re-transplanted. They were divided into 2 groups according to the usage of PGI2, i.e., non PGI2 group (n = 12) and PGI2-treated group (n = 13). In PGI2-treated group, PGI2 was administered intravenously 1 micrograms/kg/min during cooling and rewarming periods, and was added 500 ng/ml into cardioplegic solution. In the last 13 dogs (7 dogs in non PGI2 group and 6 dogs in PGI2 group) about which left ventricular functions were mainly examined, topical cooling of the myocardium was omitted. Results were as follows; compared with non PGI2 group, PGI2-treated group showed significantly higher cooling and rewarming rates, more rapid recovery of cardiac output after transplantation, and lower systemic vascular resistance throughout the experimental period. Left ventricular functions after resumption of heart beats were better in PGI2-treated group than in non PGI2 group. Microscopic examinations of the heart revealed that ischemic changes of myocardial cells were less prominent in PGI2-treated group than in non PGI2 group. It is concluded that PGI2 is useful additive for heart transplantation under deep hypothermia in that it could shorten operative time due to quicker control of the body temperature with rather stable haemodynamics and also it might protect myocardium during ischemia.
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PMID:[The role of prostaglandin I2 in heart transplantation under deep hypothermia]. 250 1

Beraprost sodium (sodium (+/-)-(1R*,2R*,3aS*,8bS*)-2,3,3a,8b-tetrahydro-2- hydroxy-1-[(E)-(3S*)-3-hydroxy-4-methyl-1-octen-6-ynyl]-1H- cyclopenta[b]benzofuran-5-butyrate, TRK-100) is an orally active epoprostenol (prostaglandin I2, PGI2) analogue. Its effect on the central nervous system (CNS) was studied. 1. When orally administered in mice, beraprost sodium at 0.3 mg/kg caused a flush of skin, a suppression of spontaneous motility, and a fall of body temperature. At 1 mg/kg and more, it showed obvious sedation, prolongation of hexobarbital hypnosis, and analgesic action in acetic acid-induced writhing test. However, even at 3 mg/kg beraprost sodium neither induced ataxia nor had anticonvulsant activity. Hypothermia was also observed in rabbits at 1 mg/kg (p.o. and i.v.). 2. When intravenously administered, beraprost sodium exerted long-lasting action on the CNS, while its pharmacological effects resembled those of PGI2. 3. Oral administration of beraprost sodium did not inhibit aggregation toxicity induced by methamphetamine (20 mg/kg i.p.) in mice. Beraprost sodium at doses higher than 1 mg/kg enhanced aggregation toxicity induced by methamphetamine (5 mg/kg i.p.), while intracerebral ventricular administration of beraprost sodium failed to enhance it. 4. In rat spinal reflex, intravenous administration of beraprost sodium (0.1 mg/kg) slightly enhanced monosynaptic reflex and at a high dose (1 mg/kg) suppressed polysynaptic reflex. 5. In the rabbit EEG, intravenous administration of beraprost sodium at a high dose (1 mg/kg) showed some effects such as the continuous pattern of wakefulness and a fall in power of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacology of beraprost sodium. 1st communication: effect on the central nervous system. 251 Jul 42

The effects of PGI2 analog (OP-41483) on hemodynamics and myocardial metabolism were compared with those of triflupromazine in dogs under simple deep hypothermia. Twenty dogs were divided into two groups according to the agent administered. In group OP (n = 10), intravenous administration of OP-41483 was performed continuously during the procedure. While the bolus of intravenous triflupromazine was injected at the beginning of cooling in group TR (n = 10). 1) Systemic and coronary vascular resistance decreased during cooling period in group OP but it increased in group TR. 2) Myocardial lactate extraction ratio was higher in group OP compared with group TR, but the ratio remained above 10% in both groups. 3) No significant differences in mean coronary blood flow and myocardial oxygen consumption were noted between the two groups. The study suggests that OP-41483 is one of the useful agents to maintain coronary circulation and myocardial metabolism under simple deep hypothermia.
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PMID:[The effects of PGI2 analog (OP-41483) on hemodynamics and myocardial metabolism during simple deep hypothermia]. 251 56

In three patients with either hypertension or Raynaud's phenomenon who were treated with different types of vasodilatory drugs, i.e. prazosin, nifedipine and prostacyclin, a decrease in rectal body temperature was measured. Overt hypothermia occurred in one patient. Because we found a pronounced improvement of arteriovenous shunt flow within the skin vessels in two of these patients, increased heat loss seems the most reasonable explanation for the observed decrease in body temperature. These observations point to an adverse effect of vasodilatory drugs. One should be aware of this possibility in patients being treated with these drugs who have complaints suggestive of hypothermia.
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PMID:Decreased rectal body temperature induced by different vasodilatory drugs. 265 56

Prostacyclin (PGI2) administered i.c.v. into the lateral rat brain ventricle in a dose of 1 and 10 micrograms causes hypothermia, catalepsy as well as a mild analgesic effect. Joint administration of PGI2 along with chloropromazine or morphine produces a greater cataleptic effect than that observed after application of neuroleptics and morphine alone. Cimetidine (CMT) (2 g/kg p.o.) administered 60 min before intraventricular PGI2 injection inhibits hypothermic and cataleptogenic action of the investigated prostaglandin. CMT blocks cataleptogenic effect of chloropromazine and morphine as well as the combination of these two substances with PGI2. CMT inhibits the cataleptogenic effect of haloperidol, but it does not block the catalepsy induced by joint administration of haloperidol and PGI2. CMT does not modify the analgesic action of PGI2. The results indicate that H2 receptors take part in some central pharmacological effects of PGI2 in rats.
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PMID:Effect of H2 receptor blockade upon hypothermic, cataleptogenic and antinociceptive action of prostacyclin (PGI)2 administered into the lateral rat brain ventricle. 286 62


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